a Base of "111 Project" for Biomechanics & Tissue Repair Engineering, Key Laboratory of Biorheological Science and Technology, Ministry of Education, Bioengineering college , Chongqing University , Chongqing , China.
b Chongqing Traditional Chinese Medicine Hospital , Chongqing , China.
Free Radic Res. 2018 Dec;52(11-12):1359-1370. doi: 10.1080/10715762.2018.1489127.
Ultraviolet A (UVA) irradiation is a potential environmental stressor, which contributes to inflammation, photoaging, and carcinogenesis. UVA causes endoplasmic reticulum stress, hence phosphorylates the α subunit of eIF2. Meanwhile, UVA also induces expression of haem oxygenase-1 (HO-1) and nuclear factor erythroid-derived two related factor 2 (Nrf2) in human skin cells. In mouse JB6 cell, we found high dose UVA could change cell morphology, cause cell viability loss. UVA irradiation activated phosphorylation of eIF2α and Nrf2-HO-1 pathway in a dose-dependent manner. Besides, modulation of eIF2α phosphorylation status could alter expression pattern of Nrf2-HO-1 signalling. Salubrinal, a selective inhibitor of eIF2α dephosphorylation, increased the S phase in cell cycle of JB6 cells after UVA irradiation, suggesting phosphorylation status of eIF2α may affect cellular homeostasis under UVA irradiation. The study directed to further acknowledge about the relationship of UVA-induced eIF2α phosphorylation and Nrf2-HO-1 pathway, which may play a role in phototherapy and photo protection.
紫外线 A（UVA）辐照是一种潜在的环境应激源，可导致炎症、光老化和致癌作用。UVA 可引起内质网应激，从而使 eIF2 的α亚基磷酸化。同时，UVA 还可诱导人皮肤细胞中血红素加氧酶-1（HO-1）和核因子红细胞衍生 2 相关因子（Nrf2）的表达。在小鼠 JB6 细胞中，我们发现高剂量 UVA 可改变细胞形态，导致细胞活力丧失。UVA 照射以剂量依赖的方式激活 eIF2α 的磷酸化和 Nrf2-HO-1 途径。此外，eIF2α 磷酸化状态的调节可改变 Nrf2-HO-1 信号的表达模式。Salubrinal 是 eIF2α 去磷酸化的选择性抑制剂，可增加 UVA 照射后 JB6 细胞的 S 期，表明 eIF2α 的磷酸化状态可能影响 UVA 照射下的细胞内稳态。该研究旨在进一步了解 UVA 诱导的 eIF2α 磷酸化与 Nrf2-HO-1 途径之间的关系，这可能在光疗和光保护中发挥作用。
